Genetic and environmental factors interact in the development of autoimmune disease in mouse and man. In the mouse, two autosomal recessive mutations, lpr, and gld, contribute to syndromes characterized by production of lymphoproliferation and autoantibodies. To evaluate mechanisms by which these mutations result in autoimmunity, we have studied the characteristics of the expanded populations of Thy-1+, CD4-, CD8-, TCR alphaB+ cells present in the lymph nodes and spleens of the mutant mice. We found that these cells do not express a cell surface molecule, CD2, present on almost all normal T cells that facilitates antigen recognition. Failure to express CD2 protein was shown to be controlled at the level of transcription.